Journal of Neuroscience, Vol 7, 760-773, Copyright © 1987 by Society for Neuroscience
Pharmacology of retinotectal transmission in the goldfish: effects of nicotinic ligands, strychnine, and kynurenic acid
RB Langdon and JA Freeman
The goal of this study was to evaluate different neurotransmitters and
their receptors that might be involved in retinotectal transmission in the
goldfish. Sections of tectum were isolated and maintained in vitro while
pharmacological agents were administered via the tissue bath. Field
potentials were elicited by electrical stimulation of the optic nerve and
recorded at 50 micron depth intervals, and profiles of current source
densities (CSDs) were computed from the second spatial derivatives of these
potentials. The preparations were treated with low [Ca2+]/high [Mg2+]
media, various cholinergic agonists and antagonists, eserine, strychnine,
or kynurenic acid, via the tissue bath. Prior to treatment, depth profiles
of these in vitro field potentials and CSDs closely resembled those
previously reported in vivo, including 2 prominent sink-source pairs with
their sinks in the superficial optic neuropil, followed by a smaller and
more prolonged sink-source pair of opposite polarity. These were rapidly
and reversibly eliminated by low [Ca2+]/high [Mg2+] bathing media, and
substantially reduced by 0.5 or 1.0 mM kynurenic acid. By contrast,
d-tubocurarine (d-TC; up to 0.16 mM) reduced peak response amplitudes by
less than 40%, eliminated the third sink-source pair, and more than doubled
the duration of decay of sink-source pairs 1 and 2 in a
concentration-dependent manner. Strychnine had a similar action to d-TC but
was slightly more potent. The time course and amplitudes of responses were
not much affected by the following nicotinic agonists or antagonists
(concentrations in microM): mecamylamine, 50; dihydro-beta-erythroidine,
50; nicotine, 200; tetramethylammonium, 500; ACh (protected by eserine,
20), 200; alpha-bungarotoxin, 2 microM for 2.5 hr, and 0.4 microM for up to
10.5 hr; and lophotoxin, 32 microM for up to 94 min. Eserine (20 microM)
and carbachol (200 microM) increased peak response amplitudes by up to 80%
within 5-10 min, and amplitudes remained elevated during 20-33 min of
continued treatment. The onset of the effects of d-TC, strychnine, and
kynurenic acid began in 5-10 min and was completed in 30 min or less,
indicating that test substances could adequately penetrate into the
interior of the isolated sections of tectum. The failure of these
cholinergic ligands to prevent postsynaptic responses indicates that
excitatory retinotectal transmission does not depend on an intact nicotinic
(or other cholinergic) system, as previously proposed. The action by
kynurenic acid suggests the involvement of an excitatory amino acid
neurotransmitter in retinotectal transmission.(ABSTRACT TRUNCATED AT 400
WORDS)
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